BackgroundThe accuracy of synovial fluid (SF) white cell count (WCC) and polymorphonuclear (PMN) cell evaluation for predicting prosthetic joint infection (PJI) at the total hip arthroplasty (THA) or total knee arthroplasty (TKA) site is unknown. Therefore, we performed a meta-analysis to summarize the diagnostic validity of SF-WCC and SF-PMN for diagnosing PJI.MethodsThe MEDLINE, EMBASE, and OVID databases were searched for studies that had evaluated the diagnostic validity of SF-WCC and SF-PMN between January 1990 and May 2013. Meta-analysis methods were used to pool sensitivity, specificity, diagnostic odd ratios (DORs), the area under the receiver-operating characteristic curve (AUC), positive likelihood ratios (PLR), negative likelihood ratios (NLR), and post-test probability. We also conducted heterogeneity, publication bias, subgroup, and meta-regression analyses.ResultsFifteen articles (15 SF-WCC and 14 SF-PMN) that included a total of 2787 patients fulfilled the inclusion criteria and were considered for analysis. The pooled sensitivity and specificity for PJI detection was 0.88 (95% confidence intervals [CI], 0.81–0.93) and 0.93 (95% CI, 0.88–0.96) for SF-WCC and 0.90 (95% CI, 0.84–0.93) and 0.88 (95% CI, 0.83–0.92) for SF-PMN, respectively. The AUC was 0.96 for SF-WCC and 0.95 for SF-PMN. PLR and NLR were 13.3 and 0.13 for SF-WCC, and 7.6 and 0.12 for SF-PMN, respectively. There was no evidence of publication bias. Low-clinical-scenario (pre-test probability, 20%) post-test probabilities were 3% for both negative SF-WCC and SF-PMN results. The subgroup analyses indicated that the sensitivity/specificity of THA were 0.73/0.96 for SF-WCC and 0.85/0.83 for SF-PMN, whereas those of TKA were 0.90/0.91 for SF-WCC and 0.90/0.88 for SF-PMN. We also found that collection of SF-WCC preoperatively had a higher sensitivity than that obtained intraoperatively (0.91 vs. 0.77).ConclusionsSF-WCC and SF-PMN have an adequate and clinically acceptable diagnostic value for detecting PJI, particularly after TKA.
Aim: To investigate the effects of plumbagin, a naphthoquinone derived from the medicinal plant Plumbago zeylanica, on human breast cancer cell growth and the cancer cell-induced osteolysis in the bone microenvironment of mice. Methods: Human breast cancer cell subline MDA-MB-231SA with the ability to spread and grow in the bone was tested. The cell proliferation was determined using the CCK-8 assay. Apoptosis was detected with Annexin V/PI double-labeled flow cytometry. Red fluorescent protein-labeled MDA-MB-231SArfp cells were injected into the right tibia of female BALB/c-nu/nu mice. Three days after the inoculation, the mice were injected with plumbagin (2, 4, or 6 mg/kg, ip) 5 times per week for 7 weeks. The growth of the tumor cells was monitored using an in vivo imaging system. After the mice were sacrificed, the hind limbs were removed for radiographic and histological analyses. Results: Plumbagin (2.5-20 μmol/L) concentration-dependently inhibited the cell viability and induced apoptosis of MDA-MB-231SA cells in vitro (the IC 50 value of inhibition of cell viability was 14.7 μmol/L). Administration of plumbagin to breast cancer bearing mice delayed the tumor growth by 2-3 weeks and reduced the tumor volume by 44%-74%. The in vivo imaging study showed that plumbagin dose-dependently inhibited MDA-MB-231SArfp cell growth in bone microenvironment. Furthermore, X-ray images and micro-CT study demonstrated that plumbagin reduced bone erosion area and prevented a decrease in bone tissue volume. Histological studies showed that plumbagin dose-dependently inhibited the breast cancer cell growth, enhanced the cell apoptosis and reduced the number of TRAcP-positive osteoclasts. Conclusion: Plumbagin inhibits the cell growth and induces apoptosis in human breast cancer cells in mice bone microenvironment, leading to significant reduction in osteolytic lesions caused by the tumor cells.
an immunophenotype and expressed IDO (AEIFN-g) consistent with ISCT guidelines, with no significant differences compared to CTR (Figure 1; p>0.05). Following co-culture at varying concentrations, both CTR and SCD MSCs equally suppressed proliferation of CTR and SCD T cells in a dosedependent manner (Figure 2; p>0.05). While a significant difference was detected between CTR and SCD MSC suppression of 3 rd party T cells (p<0.05), this was dependent on inclusion of SCD001, which had robust suppression of T cell proliferation; when this sample was removed, no significant difference was found (p>0.05). By Fluidigm array, no differences in the expression of hematopoietic factors were seen between SCD and CTR MSCs (p>0.05); stimulation with IFN
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